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首页> 外文期刊>Gastroenterology >Sulfatide-mediated activation of type II natural killer T cells prevents hepatic ischemic reperfusion injury in mice.
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Sulfatide-mediated activation of type II natural killer T cells prevents hepatic ischemic reperfusion injury in mice.

机译：硫酸酯介导的II型天然杀伤T细胞的活化可防止小鼠肝脏缺血性再灌注损伤。

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BACKGROUND & AIMS: Hepatic ischemic reperfusion injury (IRI) is a major complication of liver transplantation and resectional hepatic surgeries. Natural killer T (NKT) cells predominate in liver, where they recognize lipid antigens bound to CD1d molecules. Type I NKT cells use a semi-invariant T-cell receptor and react with alpha-galactosylceramide; type II NKT cells use diverse T-cell receptors. Some type II NKT cells recognize the self-glycolipid sulfatide. It is not clear whether or how these distinct NKT cell subsets mediate hepatocellular damage after IRI. METHODS: We examined the roles of type I and type II NKT cells in mice with partial hepatic, warm ischemia, and reperfusion injury. RESULTS: Mice that lack type I NKT cells (Jalpha18-/-) were protected from hepatic IRI, indicated by reduced hepatocellular necrosis and serum levels of alanine aminotransferase. Sulfatide-mediated activation of type II NKT cells reduced interferon-gamma secretion by type I NKT cells and prevented IRI. Protection from hepatic IRI by sulfatide-mediated inactivation of type I NKT cells was associated with significant reductions in hepatic recruitment of myeloid cell subsets, especially the CD11b(+)Gr-1(int), Gr-1(-), and NK cells. CONCLUSIONS: In mice, subsets of NKT cells have opposing roles in hepatic IRI: type I NKT cells promote injury whereas sulfatide-reactive type II NKT cells protect against injury. CD1d activation of NKT cells is conserved from mice to human beings, so strategies to modify these processes might be developed to treat patients with hepatic reperfusion injury.
机译：背景和目的：肝缺血再灌注损伤（IRI）是肝移植和切除肝脏手术的主要复杂性。自然杀伤T（NKT）细胞占肝脏，在那里它们识别与CD1D分子结合的脂质抗原。 I型NKT细胞使用半不变的T细胞受体并与α-半乳糖基胺反应; II型NKT细胞使用不同的T细胞受体。一些II型NKT细胞识别自糖脂硫酸盐。目前尚不清楚这些不同的NKT细胞亚群是如何在IRI后培养肝细胞损伤的。方法：我们检查了I型和II型NKT细胞在小鼠中具有部分肝，温度缺血和再灌注损伤的作用。结果：缺乏I型NKT细胞（JALPHA18-/ - ）的小鼠免受肝IRI的影响，通过降低肝细胞坏死和血清丙氨酸氨基转移酶的血清水平表示。硫酸酯介导的II型NKT细胞的活化通过I型NKT细胞降低干扰素-γ分泌并防止IRI。通过硫酸化物介导的I NKT细胞的肝脏灭活免受肝IRI的保护与骨髓细胞亚群，特别是CD11b（+）GR-1（int），GR-1（ - ）和NK细胞的肝脏募集中的显着降低相关。结论：在小鼠中，NKT细胞的子集在肝IRI中具有相反的作用：I型NKT细胞促进损伤，而硫酸酯反应型NKT细胞免受损伤。 CD1D活化NKT细胞与人类保存给人类，因此可以开发出改变这些过程的策略来治疗肝再灌注损伤的患者。

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